Biomedical subjects

W Craelius

Publications and source records attributed to W Craelius.

At least 19 recordsLinked to original sources

PubMed2001

Biomimetic finger control by filtering of distributed forelimb pressures.

A linear filter was developed for decoding finger commands from volitional pressures distributed within the residual forelimb. Filter parameters were based on dynamic pressures recorded from the residual limb within its socket, during specific finger commands. A matrix of signal features was derived from eight-dimensional (8-D) pressure vectors, and its pseudoinverse comprised the filter parameters. Results with amputees showed that the filter could discriminate specific finger flexion commands, suggesting that pressure vector decoding (PVD) can provide them with biomimetic finger control.

Adult↗

PubMed2000

Spectral analysis of heart variability in the newborn infant.

We investigated the relationship between spectral power and both mean heart rate (HR) and heart rate variability (HRV). Spectral power was calculated using digital heart rate recordings from term infants. Regression analysis revealed a positive correlation between low-frequency (LF) sympathetic power and HR, and a negative correlation between high-frequency (HF) parasympathetic power and HR. HRV correlated positively in all regions of the power spectrum. In awake infants, the contribution of HF power to total power (HF/TP) was significantly decreased. LF power tended to be greater, however, this trend was not statistically significant. By following expected autonomic patterns, the findings of this study confirm that spectral analysis provides a noninvasive method for the assessment of autonomic activity influencing the newborn heart. The correlation between spectral power and HRV can serve as an additional tool in the study of autonomic dysfunction.

Autonomic Nervous System↗

PubMed2000

Spectral analysis of heart rate variability in premature infants with feeding bradycardia.

An elevated level of baseline parasympathetic activity was noted in a group of premature infants suffering from bradycardia during feeding. At approximately 34 wk post-conceptional age, the heart rates of 12 infants with feeding bradycardia (birth weight = 1539 +/- 279 g; gestational age = 31.0 +/- 1.6 wk) and 10 controls (birth weight = 1710 +/- 304 g; gestational age = 32.0 +/- 1.4 wk) were recorded 1 h before and 1 h after feeding. EKG data were digitized and 3.2-min segments of data were analyzed to determine the spectral power at very low (VLF = 0.003-0.03 Hz), low (LF = 0.03-0.39 Hz), and high (HF = 0.40-1.00 Hz) frequencies. In preterm infants with feeding bradycardia, an elevation in baseline parasympathetic activity was evident before feeding, as indicated by significantly higher HF power and a lower LF/HF ratio. This elevation in baseline parasympathetic activity may contribute to the observed bradycardia during feeding.

Apgar Score↗

PubMed1999

Acute effects of thyroid hormone analogs on sodium currents in neonatal rat myocytes.

We previously reported that T3(3,3',5-triiodo-L-thyronine) acutely increases sodium currents (INa) in neonatal rat myocytes. Here we compare the effects of several thyroid hormone analogs, including T4(3,3',5,5'-tetraiodo-L-thyronine), rT3(3,3',5'-triiodo-L-thyronine), D-T3(3,3',5-triiodo-D-thyronine), 3,5-T2(3,5-diiodo-L-thyronine), DIT (3,5-diiodo-L-tyrosine), MIT (3-monoiodo-L-tyrosine), tetrac (3,3',5,5'-tetraiodo-thyroacetic acid), triac (3, 3',5-triiodo-thyroacetic acid), and tyrosine, on INa in cultured neonatal rat myocytes (n ranged from 9 to 28 for each comparison). T4, T3, 3,5-T2, and DIT (10 n m) all increased current density relative to control to a similar degree: to 1.22+/-0.2, 1.21+/-0.03, 1.16+/-0.02 and 1.16+/-0.03, respectively, P<0.05. In contrast, thyroid hormone analogs with an altered side group of the inner iodophenyl ring, including tetrac, triac, and D-T3, had no effect on INa nor did rT3, MIT or tyrosine. Pretreatment with rT3 inhibited the effects of T4, T3, 3,5-T2, and DIT. Conversely, the dose-dependent inhibitory effect of amiodarone, an iodinated benzofuran derivative that antagonizes thyroid hormone actions, on INa was blocked when myocytes were pretreated with T3(100 n m, n=3), suggesting an interaction of T3 with amiodarone. The enhancement of INa by T3 and 3, 5-T2 could not be blocked by propranolol, suggesting that the effects are not mediated through beta -adrenergic signaling pathways. In conclusion, the present results suggest that the acute effects of thyroid hormone and analogs on cardiac INa are mediated by a non-genomic thyroid hormone receptor with a unique structure-activity relationship.

Adrenergic beta-Antagonists↗

PubMed1999

A biomimetic controller for a multifinger prosthesis.

A novel controller for a multifinger hand prosthesis was developed and tested to measure its accuracy and performance in transducing volitional signals for individual "phantom" fingers. Pneumatic sensors were fabricated from open-cell polymeric foam, and were interposed between the prosthetic socket and superficial extrinsic tendons associated with individual finger flexion. Test subjects were prompted to move individual fingers or combinations thereof to execute either taps or grasps. Sensor outputs were processed by a computer that controlled motions of individual fingers on a mechanical prosthesis. Trials on three upper-limb amputees showed that after brief training sessions, the TAP controller was effective at producing voluntary flexions of individual fingers and grasping motions. Signal energies were between 5 and 25 dB relative to noise from all sources, including adjacent sensors, indicating high degrees of both sensitivity and specificity for tendon-associated transduction. Finger flexions at up to three repetitions per second, and rhythmic tapping of sequential fingers were readily transduced. One amputee subject was able to play a short piano piece with three fingers, at approximately one-quarter normal tempo. TAP sensors responded linearly to graded forces from individual fingers, indicating proportional force control. Our results demonstrate the feasibility of restoring some degree of finger dexterity by noninvasive sensing of extrinsic tendons.

Amputees↗

PubMed1997

Recognition of individual heart rate patterns with cepstral vectors.

Heart rate patterns may contain diagnostic as well as forensic information. To test these possibilities, individual heart rate patterns were represented as heart-rate cepstral vectors (HRCVs) computed in 12 dimensions via linear predictive coding (LPC) of brief segments of heart rate. A library of codebook vectors was computed for 12 cardiac patients from a standard ECG database. Statistical classification of subjects was based on the minimal weighted distances between test and codebook vectors. Weights were based on the ratio of inter- to intrasubject variances of their cepstral coefficients. Results showed that: (1) HRCV coefficients adequately reproduced the HRV spectrum, and (2) HRCV distances could be used to identify individuals within the group with a reliability of 93%. Thus, heart rate variations are an individual characteristic that can be represented as a single 12-dimensional vector.

Heart Diseases↗

PubMed1997

Cation conductance regulated by ambient Cl- in cultured rat mesangial cells.

Several functions of mesangial cells, such as contraction and release of nitric oxide, are dependent on the ambient Cl- concentration. Herein we describe a direct effect of Cl- on mesangial cell membrane conductance. Rat mesangial cells were isolated, cultured, and were patch-clamped in the whole-cell configuration. The external concentration - ([Cl-]o) - of standard Ringer's solutions was changed isotonically from standard of 160 mM to 35 mM while cell membrane conductance was continuously recorded. Results indicated that control I-V curves of the steady state current had a linear slope conductance of 0.95 nS (n = 10, r = 0.9). In low [Cl-]o, conductance outwardly rectified and increased to 4.1 nS between -120 and 0 mV and to 16.8 nS between 0 and 40 mV (n = 10, r = 0.9; p<0.01). The increase in conductance occurred within a few seconds and was reversible. Our results show that a large mesangial cell membrane conductance for cations is activated upon exposure to low [Cl-]o.

Animals↗

PubMed1995

The role of thermal feedback in electrosurgical tissue heating.

Thermal dependence of tissue resistivity was incorporated into a compartmental tissue model that predicted the interaction between power delivery from electrosurgical units (ESUs) and tissue heating. Simulations showed that as tissue resistance declines with heating, a positive feedback loop from tissue to generator is created that can promote alternate site burning. This study describes how the thermal behaviour of tissue resistance influences the output of microprocessor-controlled thermal generators, especially when used in the monopolar mode.

Computer Simulation↗

PubMed1993

Membrane currents controlled by physical forces in cultured mesangial cells.

Mechanically-activated ion channels (MACs) of cultured rat mesangial cells were stimulated by applying suction to patch pipets or by exposing cells to hypoosmotic media. MAC density was estimated as 1.5 +/- 0.4 per mu 2. In the absence of any stimulus, MAC open probabilities (N * P) were < 0.0001 increasing as a function of stretch or extracellular hypoosmolarity. Single channel mean open time during stretch increased with patch depolarization whereas hyperpolarization of the membrane delayed MAC inactivation. Ionic conductance of MACs, based on average slope conductances at hyperpolarized potentials, was 76 pS in high external K+ (N = 5) and 40 pS in high external Na+ (N = 8). PK+/PNa+ was estimated to be 4.7. MACs did not permeate Cl-, at least outwardly. Whole cell currents in response to voltage steps applied to resting cells in control conditions were approximately ohmic between -120 mV and 40 mV and were linearly and reversibly dependent on extracellular osmolarity. Our results demonstrate that: (1) MACs can be activated by both negative hydrostatic pressures applied to the pipet and by osmotic gradients; (2) MAC kinetic behavior is sensitive to membrane potential; (3) MACs may participate in cellular responses to physical forces.

Animals↗

PubMed1993

Mechanoelectrical feedback in cardiac myocytes from stretch-activated ion channels.

Stretch-activated ion channels (SAC's) in cardiac myocytes from neonatal rats were studied in cell-attached patches. Stretch of membrane patches by suction in the recording pipette caused the triggering of action potentials that were recorded as action currents (AC's). The significance of a temporal correlation between SAC open probability and AC's was tested using the Kolmogorov-Smirnov and Poisson distributions. It was shown that the 50-ms epoch immediately preceding the action current had unique kinetics and represented a peak in SAC open probability (p < 0.001). Thus it appears that current from a small number of SAC's injects sufficient charge (0.2 pC during 50 ms) to trigger action potentials in myocytes. These data strengthen the hypothesis that passive mechanical stretch of myocardium can be arrhythmogenic.

Action Potentials↗

PubMed1993

Stretch-activation of rat cardiac myocytes.

Mechanically activated ion channels (MACs) in rat ventricular myocytes were activated by stretching membrane patches attached to microelectrodes. Charge injection from MACs, consisting mainly of inward K+, was sometimes of sufficient magnitude (0.2 pC) during brief (50 ms) periods, to trigger action currents. Action currents were shown to be extracellular records of action potentials. These results demonstrate the activation of myocytes by injection of approximately 4 pA from a few MACs in a membrane patch.

Action Potentials↗

PubMed1992

Heart rate variability as an index of autonomic imbalance in patients with recent myocardial infarction.

Autonomic nervous activities are estimated in three groups of patients: Group A consists of patients who had experienced myocardial infarction (MI) within 2-6 weeks before the tests; Group B consists of patients who had MI more than one year previously; Group C consists of matched controls, free of cardiac disease. Autonomic activity is estimated using postural effects on heart rate variability (HRV): a sympathetic activity index is defined as HRV power within a low frequency band (0.04-0.12 Hz) in the tilt position and a parasympathetic activity index is defined as HRV power in a high frequency band (0.18-0.28 Hz) in the supine position. Results show that, relative to controls, Group A patients have reduced parasympathetic activity index (5 + 3 against 13 + 8, normalised units; p < 0.05) and an increased ratio of sympathetic to parasympathetic activity (17 + 17 against 4 + 2; p < 0.05). Group B is not significantly different from Group A or C. The period of 2-6 weeks post-MI thus appears to be characterised by depressed parasympathetic nervous activity which can be measured using HRV analysis.

Aged↗

PubMed1991

Acute thyroid hormone promotes slow inactivation of sodium current in neonatal cardiac myocytes.

Sodium current (INa) inactivation kinetics in neonatal cardiac myocytes were analyzed using whole cell voltage clamp before and after acute treatments with thyroid hormone (3,5,3'-triiodo-L-thyronine, T3). In untreated neonatal myocytes, INa inactivation was predominantly mono-exponential, with 93 +/- 3% (S.D.; n = 9) of the peak amplitude decaying with a time constant, tau h1, of 1.8 +/- 0.5 ms at -30 mV. The remaining 7% of control INa decayed more slowly, with a time constant, tau h2, of 9.3 +/- 3.0 ms at -30 mV. The contribution of slowly-inactivating channels to peak current was increased from 7% to 43 +/- 27% within 5 min of exposure to 5-20 nM T3 (nine cells; P less than 0.005). The time constants for both the fast- and slow-inactivating components of peak current (tau h1 and tau h2) were not significantly changed by acute T3 treatment, nor was steady-state INa inactivation (h infinity) affected. Thyroid hormone action on sodium inactivation was partially reversible by lidocaine. These findings indicate that T3 acts at the neonatal cardiac cell membrane to promote slow inactivation kinetics in sodium channels.

Animals↗

PubMed1990

Acute effects of thyroid hormone on sodium currents in neonatal myocytes.

Sodium currents and action potentials were recorded from myocytes of neonatal rats during acute exposure to thyroid hormone (5-20 nM). One to 5 minutes after addition of thyroid hormone to the bath, decay from peak Na current was slowed, with the fractional current flowing 20 ms after onset (relative to peak current) increasing from 6 +/- 5% to 17 +/- 13% (p less than 0.01, n = 12). Action potential durations were increased from 55 +/- 14 to 86 +/- 36 msec (p less than 0.05, n = 6). The effects of thyroid hormone were partially reversed by lidocaine (60 microM, n = 5), a specific blocker of a slow sub-population of Na channels. Thus thyroid hormone interacts directly with myocyte membrane, probably by slowing of inactivation of Na channels.

Action Potentials↗

PubMed1990

Use of heart rate spectral analysis to study the effects of calcium channel blockers on sympathetic activity after myocardial infarction.

We used spectral analysis of heart rate variability (HRV) to study the effects of the calcium channel blockers diltiazem and nifedipine and the beta-blocker metoprolol on the sympathetic nervous system in patients following myocardial infarction. Energy in the low-frequency range (0.04 to 0.12 Hz) in the standing (tilt) position was used as a quantitative index of sympathetic activity. Twenty-seven male patients, mean age 62 +/- 13 years, were studied 2 to 6 weeks after myocardial infarction. Eight patients received metoprolol, 100 mg twice daily; nine patients received diltiazem, 60 mg three times daily; and 10 patients received nifedipine, 10 mg three times daily. HRV and arterial blood pressure were recorded before and 5 to 7 days after initiation of therapy. None of the drugs had significant effects on the systolic blood pressure, and only nifedipine significantly reduced the diastolic blood pressure. Metoprolol and diltiazem reduced the low-frequency HRV in all patients studied, but nifedipine had no consistent effects. Our results suggest that diltiazem had a depressant effect on sympathetic activity similar to beta-adrenergic blockers. This effect was not observed with nifedipine. The reduction in sympathetic activity by diltiazem may contribute to its therapeutic effects in the post-infarction period.

Adult↗

PubMed1990

A logical state model of reentrant ventricular activation.

The ventricular surface of the heart was modeled as two-dimensional, 4096 element, network of cells connected logically to each other. An ischemic area was represented by a central core of prolonged refractoriness, distributed into eccentrically-layered elliptical contours such that refractoriness declined along varying gradients to the surrounding normal area. Propagation of cardiac action potentials was stimulated by five sequential states ranging from activation to inactivation. Reentrant activation was induced by premature stimulation of the network and resembled a "figure 8" type reentry seen experimentally. Activation patterns of reentry appeared as two propagation wavefronts which traveled around the ends of a continuous line of functional conduction block, merged into a single wavefront, then conducted slowly along a retrograde path to reactivate a region proximal to the block. Reentry could be prevented by modifying the distribution of recovery of excitability through stimulation at two strategically located sites during basic rhythm. Prevention occurred when the second site was situated in an area of prolonged refractoriness, just distal to the line of block. These simulations indicate that reentrant activation is characterized by the formation of long lines of conduction block which occur along a border of steeply graded refractoriness, and retrograde slow conduction which occurs along a more shallow refractory gradient. The occurrence of reentry is dependent on: 1) the coupling interval of the premature stimulus, 2) the location of the stimulus relative to the maximum refractory gradient, and 3) the activation sequence of the basic paced beats. Thus, this paper presents an efficient logical state model of cardiac activation which simulates experimentally observed activation patterns of reentry and its prevention.

Action Potentials↗

PubMed1990

Electrophysiological basis of ventricular late potentials.

The presence of late potentials on the body surface recording was correlated with ventricular activation maps of reentrant circuits in the postinfarction canine model of reentrant excitation. Late potentials were found to correlate with delayed myocardial activation. However, during a reentrant rhythm complete diastolic activity on the body surface could not be detected if the mass of electrically active cells was too small and/or if very slow conduction in part of the reentrant circuit generated low amplitude extracellular potentials. Myocardial zones responsible for late potentials during a basic rhythm (e.g., sinus rhythm) may not necessarily be part of the critical zone of slow conduction during reentrant activation. Dynamic changes in late potentials are not amenable to temporal signal averaging techniques but could be detected by a high resolution beat-to-beat recording. A thorough understanding of the electrophysiological limitations of late potentials in the signal-averaged ECG could result in better utilization of the technique in clinical practice as well as in the development of new approaches for the detection of the arrhythmogenic substrate.

Action Potentials↗

PubMed1989

Stretch-activated ion channels in cultured mesangial cells.

Membrane stretch, delivered by negative pressures in cell-attached patch pipettes, activated single-channel ionic currents in cultured mesangial cells. Channel opening probabilities were directly related to degree of suction, with threshold for activation being 5-10 mm Hg. The stretch-activated channels were permeable to Na+, K+, as well as Cl-, having conductances averaging 62 +/- 17 pS. These channels may represent a cellular mechano-reflex in mesangial cells.

Animals↗